Rhodococcus equi is a facultative intracellular respiratory pathogen that infects young horses and humans with acquired immunodeficiency syndrome (AIDS). In humans, R. equi is an increasingly reported opportunistic infection in immunocompromised patients, including those with AIDS. Although not currently targeted as an AIDS opportunistic infection, its impact is clear in that the number of case reports is increasing and it essentially does not occur in immunocompetent humans. Disease is insidious and results in severe cavitary pneumonia similar to Mycobacterium tuberculosis. Early diagnosis is difficult and pneumonia becomes increasingly refractory to treatment in later stages of disease. Antibiotics can reduce bacterial numbers but not effect clearance in an immunodeficient host, therefore, knowledge of immune mechanisms for R. equi clearance from the lungs would provide a basis for appropriate adjunct immunotherapy in patients with the human immunodeficiency virus (HIV). Our studies, using transgenic CD4 T cell deficient mice, demonstrate that class II restricted CD4+ T cells are required to clear R. equi infections. The goal of this proposal is to identify the CD4+ effector mechanism that mediates clearance of R. equi by 1] in vivo modulation of the CD4+ Th1 cells; 2] adaptive transfer of Th1 cells into athymic nude mice.